Differential effects on T cell and NK cell development by tissue-specific expression of H-2Dd transgene

Johansson, Maria H.; Bieberich, Charles J.; Kåse-Sjöström, Anna; Yoshioka, Takayuki; Höglund, Elin; Christy, Barbara A.; Scangos, George; Kärre, Klas; Jay, Gilbert; Höglund, Petter

doi:10.1002/1521-4141(200002)30:2<525::aid-immu525>3.0.co;2-p

Cited by 3 publications

(1 citation statement)

References 14 publications

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“…By using MHC congenic mice on the A/Sn background, we noted that the Ly49A receptor on adoptively transferred MHC‐deficient NK cells was downregulated to different extents in mice expressing H‐2 b , H‐2 a , H‐2 d and H‐2 f 20. Similarly, in a transgenic system, an H‐2L d transgene downregulated Ly49A less efficiently compared with an H‐2D d transgene, further suggesting that a single Ly49 receptor was differentially influenced by different MHC class I alleles 21. We recently confirmed these results with single MHC class I mice 10.…”

Section: A Dynamic “Rheostat” Model Of Nk‐cell Educationmentioning

confidence: 56%

Beyond licensing and disarming: A quantitative view on NK‐cell education

Brodin

Höglund

2008

Eur J Immunol

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Section: A Dynamic “Rheostat” Model Of Nk‐cell Educationmentioning

confidence: 56%

Beyond licensing and disarming: A quantitative view on NK‐cell education

Brodin

Höglund

2008

Eur J Immunol

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Chapter 2 Natural Killer Cell Tolerance

Jonsson

Yokoyama

2009

Advances in Immunology

123

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Cre Recombinase-Mediated Inactivation of H-2Dd Transgene Expression: Evidence for Partial Missing Self-Recognition by Ly49A NK Cells

Ioannidis

Zimmer

Beermann³

et al. 2001

The Journal of Immunology

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We have established H-2D(d)-transgenic (Tg) mice, in which H-2D(d) expression can be extinguished by Cre recombinase-mediated deletion of an essential portion of the transgene (Tg). NK cells adapted to the expression of the H-2D(d) Tg in H-2(b) mice and acquired reactivity to cells lacking H-2D(d), both in vivo and in vitro. H-2D(d)-Tg mice crossed to mice harboring an Mx-Cre Tg resulted in mosaic H-2D(d) expression. That abrogated NK cell reactivity to cells lacking D(d). In D(d) single Tg mice it is the Ly49A+ NK cell subset that reacts to cells lacking D(d), because the inhibitory Ly49A receptor is no longer engaged by its D(d) ligand. In contrast, Ly49A+ NK cells from D(d) x MxCre double Tg mice were unable to react to D(d)-negative cells. These Ly49A+ NK cells retained reactivity to target cells that were completely devoid of MHC class I molecules, suggesting that they were not anergic. Variegated D(d) expression thus impacts specifically missing D(d) but not globally missing class I reactivity by Ly49A+ NK cells. We propose that the absence of D(d) from some host cells results in the acquisition of only partial missing self-reactivity.

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Differential effects on T cell and NK cell development by tissue-specific expression of H-2Dd transgene

Cited by 3 publications

References 14 publications

Beyond licensing and disarming: A quantitative view on NK‐cell education

Beyond licensing and disarming: A quantitative view on NK‐cell education

Chapter 2 Natural Killer Cell Tolerance

Cre Recombinase-Mediated Inactivation of H-2Dd Transgene Expression: Evidence for Partial Missing Self-Recognition by Ly49A NK Cells

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